Mechanism of action of vitamin E in NAFLD
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ABSTRACT:
PROVIDER: PRJNA589118 | ENA |
REPOSITORIES: ENA
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Project description:Mechanism of action of vitamin E in NAFLD
| PRJNA589117 | ENA
Project description:Determine the genetic mechanism of action by which variants near PNPLA3 and LYPLAL1 exert their effects on promoting NAFLD
2018-08-02 | MSV000082692 | GNPS
Project description:Dyslipidemia and inflammation play key roles in the pathogenesis of both nonalcoholic fatty liver disease (NAFLD) and atherosclerosis. NAFLD, particularly its severe form nonalcoholic steatohepatitis (NASH) is associated with increased cardiovascular disease (CVD) risk. HDL (high density lipoprotein- also a CVD risk) are decreased in NAFLD but whether HDL function is abnormal in NAFLD is unknown. Furthermore, it is unknown whether dyslipidemia contributes to reduced HDL function in NAFLD and whether hepatic inflammation further impairs HDL function in patients with NASH. Therefore, the aim of this study was to investigate HDL function and to examine the effect of dyslipidemia and inflammation on HDL metabolism in patients with biopsy-proven simple steatosis (SS) and NASH. RESULTS: Compared to controls, SS and NASH subjects had significantly higher levels of plasma triglyceride, insulin, and were more insulin resistant (HOMA, P<0.05) with no differences in total cholesterol, HDL cholesterol, ApoB100 and ApoAI levels. NAFLD patients had increased production and degradation rates of both HDLc and ApoAI that resulted in their levels remaining stable. The degradation rates also were increased of other HDL proteins, including ApoAII, ApoAIV, vitamin D-binding protein, and complement 3 (all P<0.05). NAFLD patients had increased activities of LCAT and CETP, indicating altered HDL lipidation. NAFLD induced alterations in HDL metabolism were associated with reduced anti-oxidant but increased pro-inflammatory activity of HDL. However, no differences were observed in either HDL function or the kinetics of HDLc and HDL proteins between SS and NASH subjects.
2019-08-12 | PXD010199 | Pride
Project description:Vitamin D, in addition to calcium/phosphate metabolism and bone homeostasis regulation, has antiproliferative, anti-inflammatory and antifibrotic properties. These protective actions may have an impact in the progression of chronic liver disease including NAFLD (Non-alcoholic fatty liver disease). Vitamin D deficiency is associated with metabolic syndrome components, such as insulin resistance and dyslipidemia. NAFLD is often considered as the hepatic manifestation of metabolic syndrome, and a growing body of research suggests a relationship between vitamin D deficiency and NAFLD, with low levels of 25(OH)D associated with hepatic inflammation, and the severity and progression of NAFLD.
2022-04-14 | GSE200765 | GEO
Project description:The mechanism of action of H4 in the treatment of NAFLD.
2023-01-10 | PXD039354 |
Project description:Background: Vitamin D has been observed to affect the expression of a number of genes, however its mechanism of action has not been completely elucidated. MicroRNA molecules have recently been shown to be key mediators of gene regulation. We hypothesised therefore that vitamin D might modulate gene expression by influencing the expression of microRNAs. Methodology/Principal findings: A microRNA array was used to investigate the expression of microRNAs in RNA extracted from cells exposed to calcitriol for 0, 8 or 36 hours. A diverse panel of human cell lines were analysed including Hep-G2, HL60, K562, two fibroblast cell lines (AG09309 and AG09319), and four lymphoblastoid cell lines (GM15084, GM12878, GM07348 and GM07019). When compared between 0, 8 and 36 hours of calcitriol treatment, there were several microRNAs that were differentially regulated but the significance of these was lost after correction for multiple hypothesis testing. Conclusions/Significance: No microRNA showed significantly altered expression after exposure to vitamin D. However, some nominally significant miRNA molecules may warrant further investigation for a potential vitamin D-related role in immune function.
2010-02-02 | GSE20122 | GEO
Project description:AIMS To identify the underlying mechanism by which Vitamin D reduces colorectal cancer risk.
OBJECTIVES To demonstrate the effects of vitamin D supplementation on serum vitamin D levels.
To demonstrate dynamic changes in gene expression in response to vitamin D. To demonstrate the mechanism underlying the gene-environment interaction of vitamin D, susceptibility genetic variants (risk genes) and colorectal cancer.
| 2376099 | ecrin-mdr-crc
Project description:Investigation of the Mechanism of Action by Comprehensive Transcriptome Analysis
| PRJNA1007669 | ENA
Project description:Determine the genetic mechanism of action by which variants near PNPLA3 and LYPLAL1 exert their effects on promoting NAFLD
2017-06-05 | ST000665 | MetabolomicsWorkbench
Project description:Vitamin D is the strongest known natural anti-proliferative. A large number of studies in a wide spectrum of cancers, including epidemiological, in vitro and animal models, demonstrate that the active form of Vitamin D has anti-cancer benefits, affecting both progression and metastasis. Alike the role in calcium Vitamin D regulation, its anti-proliferative effect is thought to function through the Vitamin D receptor (VDR), although convincing evidence is lacking. Notwithstanding, separation of the calcemic and the anti-proliferative activity of Vitamin D analogues has been a major obstacle in developing new drugs for the treatment of cancer. The work presented attempts to unveil the molecular mechanism behind the anti-proliferative action of Vitamin D using genomic tools. For that purpose four independently developed Vitamin D sensitive/resistant MCF7 cell line pairs were collected. These unique biological replicates enabled us, both to increase the power of our study and to omit the use of Vitamin D. We deem this omission crucial since in the presence of Vitamin D only downstream genes involved in proliferation and cell cycle would be identified rather than causal resistance genes. The use of a variety of genomic techniques including expression, NMD and oligo CGH arrays reveal in the resistant cell lines the 11q13-14 as a region of DNA copy number loss and an altered expression of EGFR signaling pathway genes. Surprisingly, no genes known from calcium Vitamin D regulation were identified, nor did the VDR silencing by RNAi induce resistance to the sensitive cell lines. Keywords: comparative genomic hybridization, cell type comparision
2008-06-01 | GSE9887 | GEO